Neurosurgery notes/Vascular/Occlusive disease/Stroke/Cardiogenic brain embolism

Cardiogenic brain embolism

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Stroke

Numbers

  • One stroke in six is cardioembolic.

Pathology

  • Emboli may be composed of
    • Fibrin-rich thrombi (e.g. mural thrombi due to segmental myocardial hypokinesis following MI or ventricular aneurysm), OR
    • Platelets (e.g. nonbacterial thrombotic endocarditis), OR
    • Calcified material (e.g. in aortic stenosis), OR
    • Tumor particles (e.g. atrial myxoma).

Aetiology

  • Post acute myocardial infarction (AMI).
    • 2.5% of patients will have a stroke within 1–2 weeks of an AMI (the period when most emboli occur).
    • The risk is higher with anterior wall MI (≈ 6%) vs. inferior wall MI (≈ 1%).
  • Atrial fibrillation (A-fib)
    • Nonrheumatic patients with a-fib have a 3–5 fold increased risk of stroke,
      • Asymptomatic AF without tx 4.5% rate of stroke per year
      • Symptomatic AF without tx 12% rate of stroke per year
    • 75% of strokes in patients with A-fib are due to left atrial thrombi.
    • Independent risk factors for stroke in patients with A-fib are:
      • Advanced age,
      • Prior embolism (stroke or TIA)
      • HTN
      • DM, and
      • Echocardiographic evidence of left atrial enlargement or left ventricular dysfunction.
    • CHA2DS2-VASc scoring system
          • notion image
  • Prosthetic heart valves.
    • Mechanical prosthetic heart valves + long-term anticoagulation has an embolism rate of:
      • Mitral valves: 3%/year
      • Aortic valves: 1.5%/year
    • Bioprosthetic heart valves and no anticoagulation, the risk is 2–4%/year.
  • Paradoxical embolism.
    • Occur with a patent foramen ovale
      • Present in 10–18% of the general population,
    • 56% of young adults with unexplained stroke have patent foramen ovale
  • Endocarditis.
    • Evaluation
      • Blood cultures
      • TransEsophagealEcho

Diagnosis of cardiogenic brain embolism

  • Must demonstrating:
    • A potential cardiac source
    • Absence of cerebrovascular disease
    • Absence of non-lacunar stroke
  • No specific neurologic features can distinguish these patients.
  • The diagnosis is suggested in imaging studies showing multiple intracranial ischemic strokes in different arterial distributions
    • Differential diagnosis
      • Vasculitis
      • Intracranial atherosclerosis (focal plaques, more common in Asian populations that consume Western diets)
      • Intravascular lymphomatosis
  • Large areas of haemorrhagic transformation within an ischemic infarct may be more indicative of CBE due to thrombolysis of the clot and reperfusion of infarcted brain with subsequent haemorrhagic conversion.
    • Haemorrhagic transformation most often occurs within 48 hrs of a CBE stroke, and is more common with larger strokes.

Detection of cardiac source

  • Echocardiography (without transesophageal ability).
    • About 10% of patients with ischemic stroke will have potential cardiac source detected by echo, and most of these patients have other manifestations of cardiac disease.
    • In stroke patients without clinical heart disease, only 1.5% will have a positive echo; the yield is higher in younger patients without cerebrovascular disease.
  • EEG
    • AF
      • Seen in 6–24% of ischemic strokes
      • Associated with a 5-fold increased risk of stroke (see below).

Treatment

  • Only condition for which anticoagulation has been shown to significantly reduce the rate of further strokes.
  • Balance the risk of
    • Recurrent emboli (12% of patients with a cardioembolic stroke will have a second embolic stroke within 2 weeks) VS
    • Converting a pale infarct into a hemorrhagic one.
  • No study has shown a clear benefit of early anticoagulation.
  • Recommendations for anticoagulation:
    • If anticoagulation is to be used, it should not be instituted within the first 48 hrs of a probable CBE stroke
    • CT should be obtained after 48 hrs following a CBE stroke and before starting anticoagulation (to R/O haemorrhage)
    • Anticoagulation should not be used in the face of large infarcts
    • Start heparin and warfarin simultaneously. Continue heparin for 3 days into warfarin therapy, see Anticoagulation
    • Optimal range of oral anticoagulation to minimize subsequent embolism and/or hemorrhage has not been determined, but pending further data, an INR of 2–3 appears satisfactory
    • Patients with asymptomatic A-fib have 66–86% reduction in stroke risk with warfarin
      • ASA is only about half as effective
        • But may be sufficient for those without associated risk factors